Impaired glucose regulation appears to correspond with memory decline in aging, and patients with probable Alzheimer's Disease (AD) show particular abnormalities of glucose utilization and regulation. In particular, patients with probable AD show improved memory accompanied by abnormal increases in insulin during hyperglycemia. Preliminary results also show that memory is enhanced for adults with probable AD when plasma insulin levels are raised while plasma glucose is maintained at baseline. These findings suggest that disruption of baseline. These findings suggest that disruption of basic aspects of glucose regulation and utilization may contribute to memory impairment in probable AD. To further examine this hypothesis, four studies are proposed: Study 1 will determine the combined and unique effects of hyperglycemia and hyperinsulinemia on memory performance and glucoregulatory hormone levels in patients with probable AD by examining memory performance during hyperglycemia with basal insulin, during hyperinsulinemia with basal plasma glucose, and when both insulin and glucose raised to predetermined levels; Study 2 will examine dose response curves for glucose in normal elderly adults and adults with probable AD to explore previous findings that hyperglycemic memory facilitation occurs at different plasma glucose levels for some subjects with mild probable AD than for normal elderly; Study 3 will document whether longitudinal changes in glucose regulation are associated with progressive cognitive decline that characterizes probable AD as has been suggested by previous findings that changes in insulin and cortisol levels are closely associated with the progression of dementia; Study 4 will examine dose response curves for 4 different insulin infusion rates to investigate the effects of different insulin levels on memory performance in patients with probable AD and healthy elderly adults. The results of these studies will provide important information about mechanisms disrupting glucose regulation in probable AD, and about the role these mechanisms play in the cognitive deficits that characterize the disorder.